Chronic inflammation is the underlying pathophysiological mechanism of atherosclerosis. Prominent suspects being involved in atherosclerosis are lymphocytes, platelets, and endothelial cells. However, recent advances suggest a potent role for myeloid leukocytes, specifically monocyte subsets, polymorphonuclear leukocytes, and mast cells. These three cell types are not just rapidly recruited or already reside in the vascular wall but also initiate and perpetuate core mechanisms in plaque formation and destabilization. Dendritic cell subsets as well as endothelial and smooth muscle progenitor cells may further emerge as important regulators of atheroprogression. To stimulate further investigations about the contribution of these myeloid cells, we highlight the current mechanistic understanding by which these cells tune atherosclerosis.